AICAR (50mg)

Description

AICAR Peptide

Aicar peptide is an analog of adenosine monophosphate (AMP), a nucleotide that is considered to play an important role in cellular energy metabolism. It has been studied for its potential applications in research, particularly in reducing reperfusion injury after tissue ischemia and mitigating metabolic disorders. AICAR has been suggested to exert this potential by apparently activating AMP-activated protein kinase (AMPK), an enzyme that regulates various metabolic processes. AMPK potentially plays a role in restoring energy balance. It might do this by inhibiting anabolic processes: energy-consuming pathways like protein and fatty acid synthesis. Simultaneously, it might activate catabolic processes, such as the breakdown of glucose and fats, which generate ATP, thereby increasing the energy supply. There is also a possibility that AMPK influences various other cellular processes, including autophagy (the process by which cells clean out damaged components), mitochondrial biogenesis (the creation of new mitochondria), and the regulation of inflammation and stress responses. This broad range of actions suggests that AMPK might be involved in regulating several aspects of cellular and organismal function.

By potentially activating AMPK, AICAR is posited to possibly increase glucose uptake in skeletal muscle, enhance insulin sensitivity, and improve glucose tolerance. AICAR has also been suggested by researchers to have anti-inflammatory potential and may improve physical performance in certain experimental models. You may also be interested in our related research peptides, including: ghrp 2 peptide, fragment 176-191, Follistatin 344, LL-37 Peptide, Melanotan 2 Peptide, CJC-1295 DAC Peptide, Adipotide Peptide, MGF peptide, PEG-MGF Peptide ,Vilon Peptide

Chemical Makeup

Molecular formula: C₉H₁₅N₄O₈P
Molecular Weight: 338.21 g/mol
Other known titles: AICA ribonucleotide

Research and Clinical Studies

AICAR Peptide and Tissue Protection

AICAR may have organ-protective potential, especially against ischemia and reperfusion injury. The nucleotide has been suggested to potentially reduce myocardial infarction size and improve cardiac function in an animal model of myocardial ischemia-reperfusion injury.⁽¹⁾

One meta-analysis aimed to investigate the potential of AICAR on cardiovascular tissues.⁽²⁾ The data was collected from 5 randomized, placebo-controlled, double-blind clinical studies. From the results, AICAR was suggested to reduce myocardial tissue infarction size and cardiac cell death and apparently improve the overall outcome of the experiment. The study concluded that AICAR may “reduce […] adverse cardiovascular outcomes.”

Researchers posited that the apparent protective potential of AICAR may be due to its action on cellular metabolism. AICAR may potentially alter it to become more resistant to lack of oxygen by apparently upregulating the availability of energy that can be used even in anaerobic conditions. One such process is the apparent increase in the availability of myocardial glucose. To achieve that, AICAR may promote myocardial glycogenolysis (glycogen degradation) by activating AMPK. This was suggested by experiments using isolated hearts from halothane-anesthetized murine models. In these studies, AICAR appeared to increase glycogenolysis in the myocardium of murine models, while its action on glycogen synthesis was reportedly negligible. This observation hints at a potential role for AMPK activation in glycogenolysis. Further, AICAR was noted to potentially increase myocardial levels of 5-aminoimidazole-4-carboxamide 1-beta-d-ribofuranotide (ZMP), which is AICAR’s active intracellular form. However, there was no apparent change in the activity of glycogen synthase (GS) and glycogen phosphorylase (GP) in tissue homogenates, nor did AICAR seem to affect the levels of glucose-6-phosphate and adenine nucleotides in freeze-clamped tissues of these murine models. These findings suggest the possibility that ZMP might allosterically activate GP, leading to glycogenolysis in the intact hearts of the murine models, thereby providing glucose that can be used for energy even in less optimal conditions for the cells.⁽³⁾

AICAR may have protective action in other tissues as well. One study investigated the potential of AICAR, an AMPK activator, on an experimental murine model of ethanol-induced hepatic steatosis.⁽⁴⁾ The study observed that chronic ethanol exposure appeared to result in a histologically and biochemically fatty liver. Upon AICAR presentation, it appeared to attenuate the degree of change in the liver tissues. AICAR was also posited to decrease the hepatic sterol regulatory element-binding protein 1c (SREBP-1c) and reduce fatty acid synthase (FAS) enzyme expression, reducing triglyceride synthesis in murine models’ livers. SREBP-1c is posited to be a protein apparently involved in lipid metabolism, primarily in liver tissues. It is a member of the SREBP family, which appears to be transcription factors that regulate the expression of genes required to synthesize cholesterol, fatty acids, and triglycerides. Therefore, it is possible that a decrease in SREBP-1c might lead to a reduction in fatty acid synthesis. FAS is an enzyme that is considered to play a crucial role in synthesizing fatty acids. It is suggested to play a role in the process of converting acetyl-CoA and malonyl-CoA, small molecules, into palmitate, a long-chain saturated fatty acid. FAS expression also appears to be regulated by SREBP-1c.